Is Coconut Oil a Treatment for Alzheimer's Disease? We get bombarded with questions asking about Coconut Oil as a Possible Treatment Alzheimer's Disease. +Alzheimer's Reading Room It is almost like a cult, people extolling coconut oil as a treatment for Alzheimer's disease. They send emails and enter comments constantly on the Alzheimer's Reading Room. Is coconut oil an effective treatment for Alzheimer's disease? In the article below Rudy Tanzi discusses the issue and offers possible explanations of the positive affect of coconut oil on Alzheimer's patients. There is currently no peer-reviewed clinical research available regarding the efficacy of coconut oil in treating or preventing Alzheimer’s. Thanks to the Cure Alzheimer's Fund for this information. Coconut Oil: A Scientific Perspective Cure Alzheimer’s Fund has received many questions about the value of coconut oil in combatting Alzheimer’s. Rudy has agreed to provide his perspective on this, given those two giant caveats. Concerns Related Articles
New Alzheimers Care Site Promotes Community | Healthworks Collective The Alzheimer's Foundation of America (AFA) unveiled an interactive "community of care" Web site that will help family caregivers meet other caregivers, learn about the brain disorder and connect "live" with experts. Called Care Crossroads, the site addresses the feelings of isolation and stigma among Alzheimer's patients and caregivers. Caregivers are introduced to other caregivers via "I Care" video stories and creative contributions, with more of each to be posted regularly. The "House of Care" is the go-to place where visitors can click on specific rooms to learn more about strategies for behavioral challenges, recreational activities and safety issues appropriate for the specific stages of the disease. Connect: Authored by: Anthony Cirillo Anthony is the about.com expert in assisted living (assistedliving.about.com), an international healthcare consultant and a strategic partner for Answers for Elders. I work with healthcare CEOs to connect the dots in healthcare. See complete profile
Brains flush toxic waste in sleep, including Alzheimer’s-linked protein, study of mice finds While we are asleep, our bodies may be resting, but our brains are busy taking out the trash. A new study has found that the cleanup system in the brain, responsible for flushing out toxic waste products that cells produce with daily use, goes into overdrive in mice that are asleep. The cells even shrink in size to make for easier cleaning of the spaces around them. Scientists say this nightly self-clean by the brain provides a compelling biological reason for the restorative power of sleep. “Sleep puts the brain in another state where we clean out all the byproducts of activity during the daytime,” said study author and University of Rochester neurosurgeon Maiken Nedergaard. Staying up all night could prevent the brain from getting rid of these toxins as efficiently, and explain why sleep deprivation has such strong and immediate consequences. One line of thinking was that sleep helps animals to conserve energy by forcing a period of rest. Health/Science alerts
Welsh scientists make major Alzheimer’s breakthrough Researchers from Wales have helped uncover 11 new genes linked with Alzheimer’s in a major breakthrough into the causes of the disease. Scientists from Cardiff University jointly led an international collaboration gathering data from more than 74,000 people – the largest ever study of its kind – as part of a two-year project, the findings of which are published today. The academic group, headed by Merthyr Tydfil-born professor Julie Williams, has helped discover a record 11 new susceptibility genes linked with Alzheimer’s disease. It is said the breakthrough will significantly increase knowledge of the disease and lead to a better understanding of its disordered functional processes while throwing open new research avenues. Prof Williams said: “I would describe it as a significant step forward, really helping us understand what is causing the common form of Alzheimer’s disease. “This is why it has proved somewhat successful.” “They have been fantastic in their support.
Alzheimer’s Disease Completely Reversed In One Week In Mice Using New Protein Injection - RiseEarth by Arjun WaliaCollective Evolution Last year, a team of Australian researchers used a non-invasive ultrasound to assist in removing toxic plaque and lesions from nerve cells commonly associated with the onset of Alzheimer’s disease. This was a big breakthrough, as the researchers were able to reverse the processes commonly associated with the onset of Alzheimer’s, you can read more about that here. This time, researchers from the University of Glasgow, in conjunction with the Hong Kong Univeristy of Science and Technology, have discovered that one injection of a protein called IL-33 can reverse Alzheimer’s-like symptoms and cognitive decline in mice. After the injection, the mice instantly improved their cognitive function and memory, restored to that of a normal mouse within just one week of having the injections. This disease is expected to affect 65 million people by the year 2030, and developments like this are important to look at. There Is No Money In A Cure For example, Dr. Dr.
Magnesium ions show promise in slowing progression of Alzheimer's disease in mice New research published in the December 2015 issue of The FASEB Journal, shows that in mouse models of the disease oral administration of magnesium-L-threonate (MgT) alleviated cognitive decline by suppressing the Aβ deposition in amyloid plaques in an APH-1α/1β-dependent manner. Although questions still remain about how MgT permeates the blood-brain barrier, the work suggests that scientists may have found the key to a new series of Alzheimer's disease treatments. Specifically, they show that magnesium ions target pharynx defective (APH)-APH-1α/1β-suppressing the A? deposition in amyloid plaques in an anterior pharynx defective (APH)-APH-1α/1β-dependent manner. "We hope that our findings will help improve clinical practice pertinent to the optimal administration of Mg2+ for delaying or even preventing the onset of AD," said Pu Wang, Ph.D., a researcher involved in the work from the Department of Life Science and Health at Shenyang, Liaoning, China. Disclaimer: AAAS and EurekAlert!
Poor sleep linked to toxic buildup of Alzheimer's protein, memory loss Sleep may be a missing piece in the Alzheimer’s disease puzzle. Scientists at the University of California, Berkeley, have found compelling evidence that poor sleep – particularly a deficit of the deep, restorative slumber needed to hit the save button on memories – is a channel through which the beta-amyloid protein believed to trigger Alzheimer’s disease attacks the brain’s long-term memory. “Our findings reveal a new pathway through which Alzheimer’s disease may cause memory decline later in life,” said UC Berkeley neuroscience professor Matthew Walker, senior author of the study to be published Monday, June , in the journal Nature Neuroscience. Excessive deposits of beta-amyloid are key suspects in the pathology of Alzheimer’s disease, a virulent form of dementia caused by the gradual death of brain cells. “This discovery offers hope,” he said. The study was co-led by UC Berkeley neuroscientists Bryce Mander and William Jagust, a leading expert on Alzheimer’s disease.
Alzheimer's may be a collection of diseases that should be treated separately Deciphering the mechanism that underlies the development of Alzheimer's disease in certain families but not in others, researchers at the Hebrew University of Jerusalem's Faculty of Medicine have proposed that the malady is actually a collection of diseases that probably should be treated with a variety of different approaches. Neurodegenerative diseases are incurable and debilitating conditions that result in degeneration or death of cells in the nervous system. Conditions such as prion disorders (the most famous of which is "Mad Cow Disease"), Alzheimer's Disease and Parkinson's Disease share two key features: they emerge as a result of aberrant protein folding and aggregation, and their onset is late in life. These maladies emerge either sporadically or as familial, mutation-linked illnesses (certain prion disease can be also infectious). These finding raised the question of what mechanisms are negatively regulated by aging, allowing the emergence of neurodegeneration in the elderly.